研究表明肝纤维化与局部肾素血管紧张素系统(RAS)的激活有关,血管紧张素Ⅱ(AngⅡ)是 RAS中的核心效应分子,与肝星状细胞表面的相应受体ATl结合后,通过信号传导,发挥生物学效应,促进活化HSC的收缩和增殖,刺激TGF-β1 的大量表达,促进细胞外基质的生成,抑制其降解,并减少HSC凋亡,参与肝纤维化发生、发展的病理生理过程。现就AngⅡ对肝星状细胞作用的分子机制作一综述。 Studies have shown that hepatic fibrosis is associated with the activation of the renin-angiotensin system (RAS), a core effector of RAS that binds to the corresponding AT1 receptor on the surface of hepatic stellate cells Signal transduction, play a biological effect, promote the contraction and proliferation of activated HSC, stimulate the expression of TGF-β1, promote the formation of extracellular matrix, inhibit its degradation, and reduce HSC apoptosis, participate in the pathogenesis of liver fibrosis Physiological process. The molecular mechanism of Ang Ⅱ on hepatic stellate cells is reviewed.